Programmed cell death in periodontitis: recent advances and future perspectives

Song, Bin; Zhou, Ting; Yang, Wenlong; Liu, Jia; Shao, Longquan

doi:10.1111/odi.12574

Cited by 49 publications

(53 citation statements)

References 135 publications

(144 reference statements)

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“…In the current study AgP patients had higher levels of caspase‐9 compared to healthy participants ( P < 0.01). Although microbial analysis of patients with GCF was not evaluated in this study accepted as a limitation, according to the link between Aa and aggressive periodontitis, it may be suggested that Aa‐ induced apoptosis may be linked with mitochondria‐dependent intrinsic pathway in AgP.…”

Section: Discussionmentioning

confidence: 96%

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The role of caspase‐8, caspase‐9, and apoptosis inducing factor in periodontal disease

Aral

Kapila

2018

Journal of Periodontology

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Background Caspases are key mediators of apoptosis. Caspase‐8 mediates extrinsic, and caspase‐9 initiates the intrinsic pathway of apoptosis. Apoptosis Inducing Factor (AIF), a mitochondrial proapoptotic protein, mediates cell death by a caspase‐independent process. Because apoptosis is involved in periodontal disease, this study evaluated caspase‐8, ‐9, and AIF in periodontal disease. Methods Twenty periodontally healthy volunteers (Group Healthy), 20 patients with generalized aggressive periodontitis (Group AgP), and 20 patients with generalized chronic periodontitis (Group CP) were included in this study. Levels of caspase‐8, ‐9, and AIF were evaluated in gingival crevicular fluid (GCF) of all participants via enzyme‐linked immunosorbent assays. Results AIF was significantly higher in the AgP (P = 0.07) and CP groups (P = 0.01) than the Healthy group, and similar to the CP and AgP groups (P > 0.05). Caspase‐8 was significantly higher in the CP and Healthy groups than the AgP group (P = 0.00), and similar between Healthy and CP groups (P > 0.05). Caspase‐9 was significantly higher in the AgP group than the Healthy group (P = 0.01), and similar between Healthy and CP groups (P > 0.05). Conclusions The mitochondrial‐centered intrinsic pathway involving caspase‐9 and AIF, and the extrinsic pathway involving caspase‐8 are significant for aggressive periodontitis. The intrinsic pathway involving caspase‐independent AIF is also significant for chronic periodontitis.

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Section: Discussionmentioning

confidence: 96%

“…The initiation and progression phases of periodontal disease are associated with signs of apoptosis . In addition, Aa induces apoptosis in epithelial cells and macrophages, and P. gingivalis induces apoptosis in T cells .…”

Section: Introductionmentioning

confidence: 99%

The role of caspase‐8, caspase‐9, and apoptosis inducing factor in periodontal disease

Aral

Kapila

2018

Journal of Periodontology

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“…Moreover, in Chlamydia muridarum infection, RIP3 may not be involved in NLRP3 inflammasome activation, which is in contrast to what we observed following LPS/ATP stimulation of BMDMs. Currently, four distinct cellular death programs have been identified, namely, apoptosis, necroptosis, autophagy, and pyroptosis [31, 32]. Chlamydia infected cells were reported to be resistant to numerous experimental apoptotic stimuli, exhibiting inhibition of Caspase activation and blockage of cytochrome C release from mitochondria [33, 34].…”

Section: Discussionmentioning

confidence: 99%

Chlamydia muridarumInfection of Macrophages Stimulates IL-1βSecretion and Cell Death via Activation of Caspase-1 in an RIP3-Independent Manner

Chen

et al. 2017

BioMed Research International

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Chlamydiae are Gram-negative bacteria, which replicate exclusively in the infected host cells. Infection of the host cells by Chlamydiae stimulates the innate immune system leading to an inflammatory response, which is manifested not only by secretion of proinflammatory cytokines such as IL-1β from monocytes, macrophages, and dendritic cells, but also possibly by cell death mediated by Caspase-1 pyroptosis. RIP3 is a molecular switch that determines the development of necrosis or inflammation. However, the involvement of RIP3 in inflammasome activation by Chlamydia muridarum infection has not been clarified. Here, we assessed the role of RIP3 in synergy with Caspase-1 in the induction of IL-1β production in BMDM after either LPS/ATP or Chlamydia muridarum stimulation. The possibility of pyroptosis and necroptosis interplays and the role of RIP3 in IL-1β production during Chlamydia muridarum infection in BMDM was investigated as well. The data indicated that RIP3 is involved in NLRP3 inflammasome activation in LPS/ATP-stimulated BMDMs but not in Chlamydia muridarum infection. Pyroptosis occurred in BMDM after LPS/ATP stimulation or Chlamydia muridarum infection. Moreover, the results also illuminated the important role of the Caspase-1-mediated pyroptosis process which does not involve RIP3. Taken together, these observations may help shed new light on details in inflammatory signaling pathways activated by Chlamydia muridarum infection.

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“…In previous studies, depending on context, the induction of autophagy has been shown to have both protective and pathological effect in periodontitis. Song et al have comprehensively reviewed the role of autophagy in periodontitis (Song et al, 2016). In summary, autophagy may participate in periodontitis via the following mechanisms: (1) regulating periodontal pathogen invasion; (2) regulating immune signaling, resulting in inflammatory disorders and periodontal tissue damage; and (3) protecting periodontal cells from apoptosis.…”

Section: Autophagy Activation In Periodontitismentioning

confidence: 99%

The Role of Reactive Oxygen Species and Autophagy in Periodontitis and Their Potential Linkage

et al. 2017

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Periodontitis is a chronic inflammatory disease that causes damage to periodontal tissues, which include the gingiva, periodontal ligament, and alveolar bone. The major cause of periodontal tissue destruction is an inappropriate host response to microorganisms and their products. Specifically, a homeostatic imbalance between reactive oxygen species (ROS) and antioxidant defense systems has been implicated in the pathogenesis of periodontitis. Elevated levels of ROS acting as intracellular signal transducers result in autophagy, which plays a dual role in periodontitis by promoting cell death or blocking apoptosis in infected cells. Autophagy can also regulate ROS generation and scavenging. Investigations are ongoing to elucidate the crosstalk mechanisms between ROS and autophagy. Here, we review the physiological and pathological roles of ROS and autophagy in periodontal tissues. The redox-sensitive pathways related to autophagy, such as mTORC1, Beclin 1, and the Atg12-Atg5 complex, are explored in depth to provide a comprehensive overview of the crosstalk between ROS and autophagy. Based on the current evidence, we suggest that a potential linkage between ROS and autophagy is involved in the pathogenesis of periodontitis.

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Programmed cell death in periodontitis: recent advances and future perspectives

Cited by 49 publications

References 135 publications

The role of caspase‐8, caspase‐9, and apoptosis inducing factor in periodontal disease

The role of caspase‐8, caspase‐9, and apoptosis inducing factor in periodontal disease

Chlamydia muridarumInfection of Macrophages Stimulates IL-1βSecretion and Cell Death via Activation of Caspase-1 in an RIP3-Independent Manner

The Role of Reactive Oxygen Species and Autophagy in Periodontitis and Their Potential Linkage

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